Research progress on alternative non-classical mechanisms of PCSK9 in atherosclerosis in patients with and without diabetes
The proprotein convertase subtilisin/kexin type 9 (PCSK9) acts via a canonical pathway to regulate circulating low-density lipoprotein-cholesterol (LDL-C) via degradation of the LDL receptor (LDLR) on the liver cell surface. Published research has shown that PCSK9 is involved in atherosclerosis via...
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Veröffentlicht in: | Cardiovascular Diabetology 2020-03, Vol.19 (1), p.33-33, Article 33 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | The proprotein convertase subtilisin/kexin type 9 (PCSK9) acts via a canonical pathway to regulate circulating low-density lipoprotein-cholesterol (LDL-C) via degradation of the LDL receptor (LDLR) on the liver cell surface. Published research has shown that PCSK9 is involved in atherosclerosis via a variety of non-classical mechanisms that involve lysosomal, inflammatory, apoptotic, mitochondrial, and immune pathways. In this review paper, we summarized these additional mechanisms and described how anti-PCSK9 therapy exerts effects through these mechanisms. These additional pathways further illustrate the regulatory role of PCSK9 in atherosclerosis and offer an in-depth interpretation of how the PCSK9 inhibitor exerts effects on the treatment of atherosclerosis. |
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ISSN: | 1475-2840 1475-2840 |
DOI: | 10.1186/s12933-020-01009-4 |